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Deploying renewable generation to replace conventional fossil-fuel-based energy supplies provides an important pathway for the decarbonization of steelmaking plants. Meanwhile, it is also crucial to improve the flexibility of blast-furnace-gas-fired combined-cycle power plants (BFGCCs) to ease the accommodation of uncertain renewable generation. To this end, this paper proposes the deployment of a molten salt heat storage (MSHS) system in BFGCCs to store the heat of gas turbine flue gas so that the power–heat coupling of these BFGCCs can be unlocked to enhance the flexibility of the energy supply. A stochastic capacity optimization of an integrated BFGCC–MSHS–wind–solar (BMWS) energy system is presented to determine the optimal installed capacities of a BFG holder, MSHS, wind turbine, and PV panel, aiming to achieve an economic and safe energy supply for the entire system. Multiple scenarios considering uncertain fluctuations in load demands and renewable generation are generated with the Monte Carlo method based on a typical scenario. These scenarios are then reduced to representative scenarios using the synchronous substitution and reduction method for stochastic capacity optimization to enhance the reliability of the results. The case study results demonstrate that configuring MSHS reduces the total annualized cost of the BMWS system by 2.28%. Furthermore, considering the uncertainties of the power/heating load and wind/PV generation can reduce the expected annualized total cost of the BMWS system and the corresponding standard deviation by 5.66% and 81.45%, respectively. The BMWS system can achieve 730.68 tons of equivalent CO2 reduction in 24 h due to the successful utilization of renewable energy. This paper provides an effective approach for the decarbonization of energy generation systems in steelmaking plants. [ABSTRACT FROM AUTHOR]

Tooth enamel is a highly-mineralized hard tissue covering the outermost layer of the dental crown, and amelogenesis is inseparable from the participation of necessary components such as ameloblasts, organic matrix proteins, and mineral ions, such as Ca2+ and PO43-. However, mature enamel is an acellular tissue and it is difficult to self-repair once damaged. The current treatment methods for enamel damage are filling or repairing with alloys, ceramics, or composite resins. However, the mechanical properties of these materials are quite different from the natural enamel and they can’t ensure a completely closed interface with the remaining enamel surface, which usually causes a series of post-repair problems. At present, the biomimetic mineralization of tooth enamel is a research hotspot in the field of prosthodontics, and has great clinical application needs and prospects, especially the researches on cell-free strategies have made significant accomplishment. Here, based on the cell-free strategies, we review the recent knowledge from ex situ and in situ two dimensions in the remineralization of tooth ename.

Hematopoietic stem cell transplantation (HSCT) offers the highest curative potential for patients with hematological malignancies. Complications including infection, graft‐versus‐host disease (GVHD), and relapse reflect delayed or dysregulated immune reconstitution. After transplantation, NK cells rapidly reconstitute and are crucial for immune surveillance and immune tolerance. NK cell function is tightly regulated by killer immunoglobin‐like receptors (KIRs). Previous studies have revealed that donor KIRs, especially some activated KIRs (aKIRs) are closely related to transplant outcomes. Here, we performed a retrospective study, including 323 patients who received haploidentical (haplo) HSCT in our center. In univariate analysis, donor KIR2DS1, KIR2DS3 and KIR3DS1 gene protected patients with lymphoid disease from Epstein–Barr virus (EBV) and cytomegalovirus (CMV) reactivation, while donor KIR2DS1, KIR2DS5 and KIR3DS1 gene conferred a higher risk of CMV reactivation for patients with myeloid disease. Multivariate analysis confirmed that donor telomeric (Tel) B/x and KIR2DS3 gene best protected patients with lymphoid disease from EBV (p = 0.017) and CMV reactivation (p = 0.004). In myeloid disease, grafts lacking Tel B/x and KIR2DS5 gene correlated with the lowest risk of CMV reactivation (p = 0.018). Besides, donor aKIR genes did not influence the rates of GVHD, relapse, non‐relapse mortality (NRM) and overall survival (OS) in this study. The reactivation of EBV and CMV was associated with poor prognosis of haplo‐HSCT. In conclusion, we found that donor aKIR genes might have a synergistic effect on CMV and EBV reactivation after haplo‐HSCT. Whether the influence of donor aKIR genes varies with disease types remained to be studied. [ABSTRACT FROM AUTHOR]

Melatonin is an indoleamine hormone secreted by the pineal gland. It has antioxidation and anti-apoptosis effects and a clear protective effect against cardiovascular diseases. Our previous studies demonstrated that embryonic exposure to sodium arsenite (NaAsO2) can lead to an abnormal cardiac development. The aim of this study was to determine whether melatonin could protect against NaAsO2-induced generation of reactive oxygen species (ROS), oxidative stress, apoptosis, and abnormal cardiac development in a zebrafish (Danio rerio) model. We found that melatonin decreased NaAsO2-induced zebrafish embryonic heart malformations and abnormal heart rates at a melatonin concentration as low as 10−9 mol/L. The NaAsO2-induced oxidative stress was counteracted by melatonin supplementation. Melatonin blunted the NaAsO2-induced overproduction of ROS, the upregulation of oxidative stress-related genes (sod2, cat, gpx, nrf2, ho-1), and the production of antioxidant enzymes (Total SOD, SOD1, SOD2, CAT). Melatonin attenuated the NaAsO2-induced oxidative damage, DNA damage, and apoptosis, based on malonaldehyde and 8-OHdG levels and apoptosis-related gene expression (caspase-3, bax, bcl-2), respectively. Melatonin also maintained the control levels of heart development-related genes (nkx2.5, sox9b) affected by NaAsO2. In conclusion, melatonin protected against NaAsO2-induced heart malformations by inhibiting the oxidative stress and apoptosis in zebrafish. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to establish a simple, nonalcoholic fatty liver disease (NAFLD) screening model using readily available variables to identify high-risk individuals in Western Xinjiang, China., Methods: A total of 40 033 patients from the National Health Examination were divided into a training group (70%) and a validation group (30%). Univariate regression and least absolute shrinkage and selection operator models optimized feature selection, while a multivariate logistic regression analysis constructed the prediction model. The model's performance was evaluated using the area under the receiver operating characteristic curve, and its clinical utility was assessed through decision curve analysis., Results: The nomogram assessed NAFLD risk based on factors such as sex, age, diastolic blood pressure, waist circumference, BMI, fasting plasma glucose, alanine aminotransferase, platelet count, total cholesterol, triglycerides, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol. The area under the receiver operating characteristic curves were 0.829 for men and 0.859 for women in the development group, and 0.817 for men and 0.865 for women in the validation group. The decision curve analysis confirmed the nomogram's clinical usefulness, with consistent findings in the validation set., Conclusion: A user-friendly nomogram prediction model for NAFLD risk was successfully developed and validated for Western Xinjiang, China., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

Animals adapt to environmental challenges with long-term changes at the behavioral, circuit, cellular, and synaptic levels which often require new protein synthesis. The discovery of reversible N6-methyladenosine (m 6 A) modifications of mRNA has revealed an important layer of post-transcriptional regulation which affects almost every phase of mRNA metabolism and therefore translational control. Many in vitro and in vivo studies have demonstrated the significant role of m 6 A in cell differentiation and survival, but its role in adult neurons is understudied. We used cell-type specific gene deletion of Mettl14 , which encodes one of the subunits of the m 6 A methyltransferase, and Ythdf1 , which encodes one of the cytoplasmic m 6 A reader proteins, in dopamine D1 receptor expressing or D2 receptor expressing neurons. Mettl14 or Ythdf1 deficiency blunted responses to environmental challenges at the behavioral, cellular, and molecular levels. In three different behavioral paradigms, gene deletion of either Mettl14 or Ythdf1 in D1 neurons impaired D1-dependent learning, whereas gene deletion of either Mettl14 or Ythdf1 in D2 neurons impaired D2-dependent learning. At the cellular level, modulation of D1 and D2 neuron firing in response to changes in environments was blunted in all three behavioral paradigms in mutant mice. Ythdf1 deletion resembled impairment caused by Mettl14 deletion in a cell type-specific manner, suggesting YTHDF1 is the main mediator of the functional consequences of m 6 A mRNA methylation in the striatum. At the molecular level, while striatal neurons in control mice responded to elevated cAMP by increasing de novo protein synthesis, striatal neurons in Ythdf1 knockout mice didn't. Finally, boosting dopamine release by cocaine drastically increased YTHDF1 binding to many mRNA targets in the striatum, especially those that encode structural proteins, suggesting the initiation of long-term neuronal and/or synaptic structural changes. While the m6A-YTHDF1 pathway has similar functional significance at cellular level, its cell type specific deficiency in D1 and D2 neurons often resulted in contrasting behavioral phenotypes, allowing us to cleanly dissociate the opposing yet cooperative roles of D1 and D2 neurons.